Discovery of New Isotopes

Using the fusion-evaporation reaction ^{106}Cd(^{58}Ni,4n)^{160}Os and the gas-filled recoil separator SHANS, two new isotopes _{76}^{160}Os and _{74}^{156}W have been identified. The α decay of ^{160}Os, measured with an α-particle energy of 7080(26) keV and a half-life of 201_{-37}^{+58} µs, is assigned to originate from the ground state. The daughter nucleus ^{156}W is a ß^{+} emitter with a half-life of 291_{-61}^{+86} ms. The newly measured α-decay data allow us to derive α-decay reduced widths (δ^{2}) for the N=84 isotones up to osmium (Z=76), which are found to decrease with increasing atomic number above Z=68. The reduction of δ^{2} is interpreted as evidence for the strengthening of the N=82 shell closure toward the proton drip line, supported by the increase of the neutron-shell gaps predicted in theoretical models.

Evidence for Chiral Wobbler in Nuclei.

Three ΔI=1 bands with the πg_{9/2}⊗νg_{9/2} configuration have been identified in _{35}^{74}Br_{39}. Angular distribution, linear polarization, and lifetime measurements were performed to determine the multipolarity, type, mixing ratio, and absolute transition probability of the transitions. By comparing these experimental observations with the corresponding fingerprints and the quantum particle rotor model calculations, the second and third lowest bands are, respectively, suggested as the chiral partner and one-phonon wobbling excitation built on the yrast band. The evidence indicates the first chiral wobbler in nuclei.

Occupancy of orbitals and the quadrupole collectivity in 45Sc nucleus.

In the present work, the Doppler Shift Attenuation method (DSAM) was used to analyze the observed lineshapes of transitions from excited states in 45Sc, populated in the reaction 36Ar + 12C at a beam energy of 145 MeV. The interpretation and comparison of the experimental results have been performed with large-scale shell model calculations, involving different interactions like: GX1A, GX1J, FPD6, KB3 and ZBM2. KB3 and FPD6 (present work) interactions in the negative parity states, and in positive parity states ZBM2 are most pre-eminent in reproducing the results, due to the large configuration space describing strong collective effects. Furthermore, the present work also looks at the details of the shell model helping in improving the understanding for the occupancy of orbitals. The present investigation suggests the observation of stronger collectivity for positive parity states over negative parity states with predicted enhanced collectivity of states in 45Sc nucleus.

Probing

The isomer depletion of ^{93m}Mo was recently reported [Chiara et al., Nature (London) 554, 216 (2018)NATUAS0028-083610.1038/nature25483] as the first direct observation of nuclear excitation by electron capture (NEEC). However, the measured excitation probability of 1.0(3)% is far beyond the theoretical expectation. In order to understand the inconsistency between theory and experiment, we produce the ^{93m}Mo nuclei using the ^{12}C(^{86}Kr,5n) reaction at a beam energy of 559 MeV and transport the reaction residues to a detection station far away from the target area employing a secondary beam line. The isomer depletion is expected to occur during the slowdown process of the ions in the stopping material. In such a low γ-ray background environment, the signature of isomer depletion is not observed, and an upper limit of 2×10^{-5} is estimated for the excitation probability. This is consistent with the theoretical expectation. Our findings shed doubt on the previously reported NEEC phenomenon and highlight the necessity and feasibility of further experimental investigations for reexamining the isomer depletion under low γ-ray background.

Tertiary dentinogenesis with calcium hydroxide: a review of proposed mechanisms.

Calcium hydroxide has been used extensively in dentistry for a century. Despite its widespread use as a pulp-capping agent, its mechanisms of action still remain ambiguous. Understanding its modes of action will lead to a broader understanding of the mechanisms associated with induced dentinogenesis and help in optimizing the currently available agents to target specific regenerative processes to obtain the best possible clinical outcomes. A literature search relating to mechanisms of dentinogenesis of calcium hydroxide up to December 2011 was carried out using pubmed and MEDLINE database searches as well as manual searching of cross-references from identified studies. Resulting suggestions regarding dentinogenic mechanisms of calcium hydroxide range from direct irritating action of the material to induction of release of biologically active molecules. The purpose of this article is to discuss various mechanisms through which calcium hydroxide may induce tertiary dentinogenesis in the light of observations made in included studies.

Alterations in macromolecular composition and cell wall integrity by ciprofloxacin in Mycobacterium smegmatis.

The present study has been undertaken to explore the biochemical mechanism of antimycobacterial action of a potent fluoroquinolone i.e. ciprofloxacin in Mycobacterium smegmatis. Cells grown in the presence of a subinhibitory concentration (IC50) of ciprofloxacin had a significantly lower content of all the major macromolecules i.e. DNA, RNA, proteins and lipids with maximum inhibition in DNA concentration as compared to control. Significant quantitative changes were also observed in the various chemical constituents of cell wall of ciprofloxacin grown cells. A decrease in the number of binding sites for a fluorescent probe L-anilinonapthalene-8-sulphonate (ANS) in ciprofloxacin grown cells suggested structural changes on the cell surface. Significant changes were also observed in the morphology of cells grown in the presence of ciprofloxacin by scanning electron microscopy (SEM). Our results suggest that ciprofloxacin exerts its antimycobacterial activity by affecting the cell wall as well as various macromolecules, particular DNA, the vital component for cell survival and growth.

Insulin internalization in the absence of the insulin receptor tyrosine kinase domain is insufficient for mediating intracellular biological effects.

The intracellular portion of the human insulin receptor (hIR) beta-subunit contains distinct functional domains including the exon 16-encoded juxtamembrane (JM) domain that mediates endocytosis, and the tyrosine kinase (TK) domain that mediates insulin's metabolic and mitogenic actions. To explore the functional relationship between these domains and to determine the role of insulin internalization in insulin action, we constructed and studied the endocytic and signaling properties of an hIR mutant truncated at Glu-1012. This truncation removes the carboxyl-terminal 343 amino acids containing essentially all of the TK domain but leaves behind the exon 16-encoded JM domain that is necessary for endocytosis, plus an additional 35 amino acids downstream. The wild-type (hIR-WT) and mutant (hIR delta 343) receptors were stably expressed in CHO cells and their abilities to mediate various insulin-stimulated functions were comparatively analyzed. In cells expressing hIR-WT, insulin markedly enhanced tyrosine phosphorylation of the beta-subunit and of the endogenous 185 kDa substrate whereas these effects were completely absent in cells expressing hIR delta 343. The hIR delta 343 receptors retained the ability to internalize a significant amount of surface-bound insulin at 37 degrees C. However, they were unable to mediate either the short or long-term biological effects of insulin as determined by assaying insulin-stimulated glucose uptake (assessed by 2-deoxyglucose uptake), protooncogene expression (measured by Northern blot analysis of c-fos mRNA) and DNA synthesis (measured by 3H-thymidine incorporation). These results indicate that the hIR beta-subunit JM and TK domains can be functionally uncoupled, and that insulin internalization in the absence of hIR TK domain and kinase activity is insufficient for mediating intracellular insulin action.

Insulin downregulates the steady-state level of its receptor's messenger ribonucleic acid.

The effects of insulin on the steady-state level of human insulin receptor (hIR) mRNA were examined in the HepG2 human liver cell line using Northern blot analysis of either total cellular or poly(A)+ RNA. In control cells, up to six (4.5, 5.2, 7.4, 8.5, 9.4 and 10.8 kb) hybridizable species of hIR mRNA were identified, with the 8.5 and 10.8 kb species being most prominent. Incubation for 18 hrs with 1 microM insulin resulted in a similar decrease (to approximately 35% of control) of all the hIR mRNA species. The insulin effect was dose-dependent and was half-maximal by 2-3 hrs and maximal by 4-6 hrs of incubation at 37 degrees C. The hIR mRNA levels remained maximally insulin suppressed for up to 18 hrs but thereafter the effect became attenuated. These results indicate that insulin downregulates the level of hIR mRNA with a biphasic time-course and that this process is most likely part of the general mechanism by which insulin maintains the homeostatic control of its cellular receptor levels.

Replacement of the human insulin receptor transmembrane and cytoplasmic domains by corresponding domains of the oncogene product v-ros leads to accelerated internalization, degradation, and down-regulation.

Internalization, degradation, and insulin-induced down-regulation of insulin receptors were studied comparatively in transformed Chinese hamster ovary (CHO) cell lines, CHO.T and CHO.IR.ros, respectively expressing either the wild-type human insulin receptor (hIR) or a mutated hybrid receptor in which the transmembrane and cytoplasmic domains of hIR were replaced by corresponding domains of the transforming protein p68gag-ros (v-ros) of avian sarcoma virus UR2. At 37 degrees C, degradation of insulin receptors photoaffinity labeled on the cell surface (440 kDa) was most rapid for the hybrid hIR.ros (t1/2 1.0 +/- 0.1 h), intermediate for the wild-type hIR (t1/2 2.7 +/- 0.5 h), and slowest for the endogenous CHO insulin receptors (t1/2 3.7 +/- 0.7 h). Initial intracellular accumulation of the hIR.ros hybrid was also most rapid, reaching maximal amounts in 20 min following which the receptors disappeared rapidly from the intracellular compartment. In contrast, intracellular accumulation of the receptors in the CHO.T and CHO cells was slower, reaching maximal amounts in 60 min, and rapid disappearance of the receptors from the intracellular compartment did not occur. Chloroquine, a lysosomotropic agent, inhibited degradation of both the wild-type hIR and the chimeric hIR.ros and increased their intracellular accumulation. However, the chloroquine effect was much more marked for the hIR.ros receptors whose intracellular accumulation was increased by greater than 300% (in comparison with approximately 60% increase for the wild-type hIR), demonstrating marked intracellular degradation of the hybrid hIR.ros at chloroquine-sensitive sites. Insulin-induced down-regulation of the cell surface hIR.ros (52% loss in 3 h) was also more marked than the wild-type hIR (approximately 30% loss in 3 h). Thus, in the hybrid hIR.ros receptor, which was shown previously to exhibit insulin-stimulated autophosphorylation and kinase activity but not insulin-stimulated metabolic function, the capacity for internalization and down-regulation is not only preserved but is also markedly accelerated. These findings suggest that 1) the postreceptor coupling mechanisms mediating insulin-induced receptor internalization, degradation, and down-regulation are different from those mediating metabolic functions; and 2) v-ros may contain the structural information directing accelerated receptor catabolism.